1528 Letters to the Editor December 1987

American Heart Jwrnal

Table I. Joint association of serum cholesterol and cigarette smoking with coronary mortality in 6 years -.-___.__

Cigarette smokers Nonsmokers INS) ___- Difference Ratio of

Serum cholesterol No. CHD Rate/ No. CHD Rate/ in rates rates quintile (mgldl) Total deaths 1,000 Total deaths 1,000 (smokers-NS) (smokPrsfNS)

Ql (<182) 21,102 107 5.07 41,512 93 2.24 2.83 2.26 Q2 (182-202) 22,583 164 7.26 42,639 146 3.42 3.84 2.12 Q3 (203-220) 22,759 229 10.06 41,518 191 4.60 5.46 2.19 $4 (221-244) 24,245 315 12.99 41,766 255 6.11 6.88 2.13 Q5 (>244) 26,214 474 18.08 41,046 452 11.01 7.07 1.64 Total 116,903 1,289 11.03 208,481 1.137 5.45 5.58 2.02

____-

The absence of an interaction when the logit model is used is also apparent when considering the regression coefficients corre- sponding to serum cholesterol concentration for nonsmokers and smokers based on a separate logistic regression analyses. These parameter estimates are 0.0076 and 0.0070 for nonsmokers and smokers, respectively. One can use the estimated regression coefficient corresponding to serum cholesterol to estimate the increased risk of CHD death associated with an assumed increase of 10 mg/dl of cholesterol, for exaniple. For nonsmokers, the risk of death from CHD in 6 years is increased by 7.9%; for smokers it is increased by 7.0%. Since the CHD death rate for smokers is approximately two times greater than that for nonsmokers and since these estimated percentage changes in CHD risk based on the logistic model are similar, the expected difference in CHD rates resulting from the cholesterol increase is approximately two times greater for smokers than for nonsmokers. In this case, the absence of an interaction on the logit scale implies that one must exist when a linear model is used.

In other analyses in our report, the joint relationship of serum cholesterol, cigarette smoking, and diastolic blood pressure with death from CHD was summarized with the use of a logistic model (see Table VIII, for example). This model was used since it provides a simple description of the data based on an additive model and because the resulting model is more generalizable from one group of participants to another (note the similarity of the regression coefficients corresponding to serum cholesterol for MRFIT and Framingham white men in Table IX, for example).

James D. Neaton, Ph.D., Division of Biometry

University of Minnesota 2829 University Ave., SE.

Suite 508 Minneapolis, MN 55414-3270

on behalf of: W. B. Kannel, M.D., M.P.H.

D. Wentworth, M.P.H.

H. E. Thomas, M.D. J. Stamler, M.D.

S. B. Hulley, M.D., M.P.H. M. 0. Kjelsberg, Ph.D.

3. Walter SD, Holford TR. Additive, multiplicative, and other models for disease risks. Am J Epidemiol 1978;108:341-6.

CORONARY RUPTURE AND PTCA

To the Editor: Goldman et al. present an interesting case of surgically reme-

died rupture of a coronary artery during percutaneous translumi- nal angioplasty.’ In it, they claim that theirs is the “first angiographically documented report of nonfatal arterial rupture associated with PTCA.” We would like to point out that our previously reported case of cardiac tamponade due to the rupture of a diagonal branch of the left anterior descending coronary artery during angioplasty’ was not only nonfatal, but was success- fully treated with pericardiocentesis and other supportive mea- sures without coronary bypass surgery. In this patient, the dilatation of the left anterior descending artery was successful, the patient sustained no myocardial damage, and is presently doing well 30 months later.

John Wertheimer, M.D. S. Yazdanfar, M.D.

Morris N. Kotler, M.D. Albert Einstein Medical Center

York and Tabor Roads Philadelphia, PA 19141

REFERENCES

1. Goldman MH, Masden RR, Yared S. Acute rupture of the left anterior descending coronary artery secondary to percutane- ous transluminal angioplasty. AM HEART J 1986;112:1325-8.

2. Altman F, Yazdanfar S, Wertheimer J, Ghosh S, Kotler M. Cardiac tamponade following perforation of the left anterior descending coronary system during percutaneous translumi- nal coronary angioplasty: successful treatment by pericardial drainage. AM HEART J 1986;111:1196-7.

REPLY

REFERE&CES To the Editor:

Kannel WB, Neaton JD, Wentworth D, Thomas HE, Stamler J, Hulley SB, Kjelsberg MO. Overal and coronary heart disease mortality rates in relation to major risk factors in 325,348 men screened in MRFIT. AM HEART J 1986;112:825- 36. Rothman KJ. The estimation of synergy or antagonism. Am J Epidemiol 1976;103:506-11.

I’d like to thank Drs. Wertheimer, Yazdenfar, and Kotler for alerting me to their case report concerning perforation of a diagonal branch during balloon angioplasty (their report was unpublished at the time of preparation of our manuscript), Given the details of their case report and the illustrations provided, it would seem likely that the small diagonal branch was perforated with the stiff tip of the exchange wire, though the authors felt

Volume 114

Number 6 Letters to the Editor 1529

that the likely explanation was inadvertent dilation of the small branch. I base this opinion on the distance of the dilation site as well as the location of the wire outside the coronary lumen. Fig. 2, I believe, does show guidewire perforation. It would be helpful to have another view to further document the wire’s position. Given the above considerations, I feel our report represents a rupture and not perforation of a major epicardial vessel. Small perfora- tions of septal and diagonal branches are usually tolerated. Dr. Wertheimer’s case represents an untoward effect of perforation. I believe that it is important that such anecdotal information be published to inform physicians of such complications and the varying outcomes of medical as well as surgical therapy.

Michael Goldman, M.D. Cardiovascular Consultants 616 Medical Towers North

233 East Gray Street Louisville, KY 40202

ANTERIOR PLUS INFERIOR MYOCARDIAL INFARCTION AND SINGLE-VESSEL DISEASE

To the Editor: Janosik et al.’ reported anterior and inferior myocardial infarc-

tion in a young woman with angiographically normal coronary arteries. Vasospasm of multiple coronary arteries was proposed as a mechanism for the myocardial infarction. Although the mecha- nism was probably coronary vasospasm, there is no need to involve multiple coronary arteries in order to explain the concom- itant inferior and anterior myocardial infarction.

Recently we treated a patient who presented to our Coronary Care Unit with precordial pain. The ECG was typical for acute anterior and inferior myocardial infarction. Because of severe post myocardial infarction angina, he was catheterized. Left ventriculography demonstrated akinesis of the anterolateral wall and inferoapical segment. Selective coronary angiography revealed a 90% proximal narrowing of the left anterior descend- ing artery that “wrapped around the apex.” Otherwise, the coronary circulation was normal. Our case shows that involve- ment of a long left anterior descending vessel might cause anterior and inferior myocardial infarction because the artery supplies the anterior as well as a part of the inferior wall. This fact had already been described by Williams et al.’ in 1973. From the angiograms of Janosik et al., we could not determine if the left anterior descending coronary artery “wrapped around the apex.” If “apex wrap-around” did exist, that might explain the simulta- neous anterior and inferior myocardial infarction.

Reuben Ilia, M.D. Ilya A. Ovsyshcher, M.D. Benjamin Goldfarb, M.D.

Department of Cardiology Soroka Medical Center

Beer-Sheba, Israel

REFERENCES

1. Janosik DL, Labovitz AJ, Kennedy HL. Anterior and inferior msocardial infarction in a voung woman with anaiograuhical- ly-normal coronary arteries. Ai HEART J 1986;1?2:606.

2. Williams RA. Cohn PF. Vokonas PS. Youne E. Herman MV. Gorlin R. Electrocardiographic, arteriographic’ and ventricu: lographic correlations in transmural myocardial infarction. Am J Cardiol 1973;31:595.

REPLY

To the Editor: We recognize the fact that a left anterior descending coronary

artery that wraps around the apex may supply the inferior as well as the anterior ventricular segment and that disease of this type of artery could cause simultaneous anterior and inferior myocar- dial infarction. However, the patient we described did not have a long left anterior descending artery that wrapped around the apex. This may not he apparent from the limited angiographic views supplied in the case report. Furthermore, a two-dimension- al echocardiogram and contrast left ventriculography in the left anterior oblique projection demonstrated severe hypokinesis of the posterior and posterolateral walls, in addition to akinesis of the anterior and inferoapical segments, implicating both the left anterior descending and right coronary arteries in this patient’s myocardial infarction.

Denise L. Janosik, M.D. Division of Cardiology

St. Louis University Medical Center 1325 S. Grand Blvd. St. Louis, MO 63104

ETIOLOGIC SPECTRUM OF CONSTRICTIVE PERICARDITIS

To the Editor: Cameron et al.’ have made a solid contribution to updating the

etiologic spectrum of constrictive pericarditis. It not only agrees with qualitative observations,* but also provides a statistical framework applicable to referral centers. The authors may wish to amplify their observations by clarifying certain attractive data that are not examined. Pulsus paradoxus and Kussmaul’s sign are noted respectively in 16% and 13% of their series. In both classic constriction and pure cardiac tamponade, these two entities should be mutually exclusive; therefore, would the authors address the following questions? (1) How was pulsus paradoxus defined? (2) Was lung disease (another notorious cause of pulsus paradoxus) excluded in their patients? Finally, (3) Was there any residual fluid accompanying constriction in some patients? The latter would be related to what was first described as “subacute constrictive pericarditis with cardiac tamponade”’ (better described by Hancock’ as “effusive-constrictive pericarditis”). It is possible that in the older literature, some of which included pulsus paradoxus as a sign in constrictive pericarditis, the presence of lung disease or significant pericardial fluid was not rigorously excluded.

One can agree that povidone-iodine was the most likely irritant in producing post surgical contriction, since it was long ago pointed out’ that the constituents of this irrigant had been used to produce experimental constrictive pericarditis. On the other hand, could there have been a role for talc (i.e., would enough have remained on the surgeon’s gloves)? The authors also felt the reason for higher mortality was unclear in the subgroup with post radiotherapy constriction. Had they allowed for the presence of malignant disease in these patients as opposed to other etiolog- ies? These comments are not meant in direct criticism, but rather to request amplification of an excellent contribution.

David H. Spodick, M.D. Cardiology Division

Saint Vincent Hospital Worcester, MA 01604